Summary Excess soluble salts in soil are harmful to the growth and development of most plants. Evidence is emerging that the plant cell wall is involved in sensing and responding to salt stress, but the underlying mechanisms are not well understood. We reveal that the histone acetyltransferase General control non‐repressed protein 5 (GCN5) is required for the maintenance of cell wall integrity and salt stress tolerance. The levels of GCN5 mRNA are increased in response to salt stress. The gcn5 mutants exhibited severe growth inhibition and defects in cell wall integrity under salt stress conditions. Combining RNA sequencing and chromatin immunoprecipitation assays, we identified the chitinase‐like gene CTL1, polygalacturonase involved in expansion‐3 (PGX3) and MYB domain protein‐54 (MYB54) as direct targets of GCN5. Acetylation of H3K9 and H3K14 mediated by GCN5 is associated with activation of CTL1, PGX3 and MYB54 under salt stress. Moreover, constitutive expression of CTL1 in the gcn5 mutant restores salt tolerance and cell wall integrity. In addition, the expression of the wheat TaGCN5 gene in Arabidopsis gcn5 mutant plants complemented the salt tolerance and cell wall integrity phenotypes, suggesting that GCN5‐mediated salt tolerance is conserved between Arabidopsis and wheat. Taken together, our data indicate that GCN5 plays a key role in the preservation of salt tolerance via versatile regulation in plants.

Polyploidy occurs prevalently and plays an important role during plant speciation and evolution. This phenomenon suggests polyploidy could develop novel features that enable them to adapt wider range of environmental conditions compared with diploid progenitors. Bread wheat (Triticum aestivum L., BBAADD) is a typical allohexaploid species and generally exhibits greater salt tolerance than its tetraploid wheat progenitor (BBAA). However, little is known about the underlying molecular basis and the regulatory pathway of this trait. Here, we show that the histone acetyltransferase TaHAG1 acts as a crucial regulator to strengthen salt tolerance of hexaploid wheat. Salinity-induced TaHAG1 expression was associated with tolerance variation in polyploidy wheat. Overexpression, silencing and CRISPR-mediated knockout of TaHAG1 validated the role of TaHAG1 in salinity tolerance of wheat. TaHAG1 contributed to salt tolerance by modulating ROS production and signal specificity. Moreover, TaHAG1 directly targeted a subset of genes that are responsible for hydrogen peroxide production, and enrichment of TaHAG1 triggered increased H3 acetylation and transcriptional upregulation of these loci under salt stress. In addition, we found the salinity-induced TaHAG1-mediated ROS production pathway is involved in salt tolerance difference of wheat accessions with varying ploidy. Our findings provide insight into the molecular mechanism of how an epigenetic regulatory factor facilitates adaptability of polyploidy wheat and highlights this epigenetic modulator as a strategy for salt tolerance breeding in bread wheat.

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Common wheat (Triticum aestivum L.) is an important staple food crop worldwide. Lateral roots (LRs), as the major component of root architecture, affect water and nutrient uptake in wheat. The phytohormone ethylene is known to affect LR formation; however, the factor(s) modulating ethylene during this process have not yet been elucidated in wheat. Here we identified wheat TaWRKY51 as a key factor that functions in LR formation by modulating ethylene biosynthesis. Wheat TaWRKY51RNA interference lines (TaWRKY51-RNAi) and the homozygous mutants tawrky51-2a and tawrky51-2b all produced fewer LRs than the wild type and negative transgenic plants, whereas the TaWRKY51 overexpression lines (TaWRKY51-OE) had the opposite phenotype. Transcription analysis revealed that 1-aminocyclopropane-1-carboxylic acid synthase (ACS) genes (TaACS2, TaACS7 and TaACS8) involved in ethylene biosynthesis were downregulated in TaWRKY51-OE lines but upregulated in TaWRKY51-RNAi lines. The rate of ethylene production also decreased in TaWRKY51-OE lines but increased in TaWRKY51-RNAi lines compared with their respective negative transgenic controls. Electrophoretic mobility shift and transient expression assays revealed that TaWRKY51 inhibits the expression of ACS genes by binding to the W-box cis-element present in their promoter region. Moreover, overexpression of ACS2 or exogenous application of 1-aminocyclopropane-1-carboxylic acid reversed the phenotype of enhanced LR number in TaWRKY51-OE Arabidopsis lines, and overexpression of TaWRKY51 in the ethylene-overproducing mutant eto1-1 rescued its LR defect phenotype. In addition, genetic evidence demonstrates that TaWRKY51-regulated LR formation is also dependent on ethylene and auxin signaling pathways. Our findings reveal a molecular genetic mechanism by which a WRKY gene coordinates ethylene production and LR formation in wheat.